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However, no steroid has eliminated the androgenic effects because the so-called androgenic effects are really anabolic effects in sex-linked tissues(Fig. 9). This is because the testosterone levels induced by the androgenic effect are inversely related to the levels of estradiol (a primary metabolite of testosterone). Indeed, if the androgen activity was blocked, there would be no effect on estradiol. On the other hand, there is evidence that androgens in the presence of estradiol can stimulate the growth of androgen-receptor positive cells. As a result, the concentration of androgens in the blood would be higher than normal after androgen exposure. Such an effect is called suppression of the androgenic effect.Finally, there is a third androgen-receptor positive cell type that contains the androgen receptor: these cells are not sexually dimorphic in their morphologies, and they are in the nucleus of the testis. The presence of the testosterone in the cells is a sexually dimorphic androgen response that is blocked by androgens. In our study, when mice were treated with the progesterone analogue (i.p. injection of the progesterone) for several weeks, which has been proposed as a way of inducing the "anti-androgenic" effects of progesterone in humans, the effect was inhibited. Therefore, it is very likely that there are sex-linked sex differences in the responses of these cells to stimulation of the testis (Fig. 9, p. 16).This study offers important insights to further understanding of the pathophysiology of testicular disease. These observations do not indicate that androgenic hormones in excess could result in testicular malignancy. For example, the data suggest that androgen-stimulated testicular atrophy could be an important cause of testicular cancer. This is because androgen-stimulated testicular atrophy is inversely related to the level of estradiol concentrations. These data show that androgen-stimulated testicular atrophy is not a sexually "normal" consequence of testosterone.Similar articles: